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Chronic inflammation promotes cancer progression as a second hit
Monika Burocziova1, Srdjan Grusanovic2, Karolina Vanickova3
1Laboratory of Hemato-oncology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
Experimental Hematology
|September 14, 2023
Summary
Chronic inflammation can drive acute myeloid leukemia (AML) development, even without a second mutation. Elevated cytokines and Jak/Stat3 pathway activation in inflammation may replace genetic hits, accelerating AML.
Area of Science:
- Hematology
- Oncology
- Immunology
Background:
- Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow.
- The "two-hit" theory suggests AML arises from cooperating driver mutations.
- Some AML cases have only one driver mutation, leaving transformation mechanisms unclear.
Purpose of the Study:
- To investigate the role of chronic inflammation in AML development.
- To determine if non-genetic factors can substitute for a "second hit" mutation in AML.
Main Methods:
- Utilized a mouse model of chronic inflammation.
- Analyzed systemic cytokine and chemokine levels.
- Assessed Jak/Stat3 signaling pathway activation.
Main Results:
- Chronic inflammation led to elevated cytokines and chemokines.
- Hyperactivation of the Jak/Stat3 pathway was observed.
- These inflammatory changes accelerated leukemic transformation in the mouse model.
Conclusions:
- Chronic inflammation can act as a "second hit" in AML development.
- Inflammatory pathways, like Jak/Stat3, contribute to leukemogenesis.
- Findings offer new insights into AML mechanisms and potential therapeutic targets.
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